Rad Onc Twitter

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Isn’t he big on residency expansion?
He definitely thinks we need to get paid closer to pediatricians, a comment he made on Twitter a couple years ago 🤷🏾.

Happy to lift all boats (I do think peds is underpaid) but that doesn't mean letting boomers ride the good times and telling the rest of us that we are paid too much.

Regarding expansion I think he's always looked for reasons not to contract spots, data be damned, and that by overtraining more we will somehow have more docs to strengthen the specialty 🙄 Haven't paid enough attention to UC residency numbers to find out whether he has been blatantly expanding as much as some other places have been

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Under usual scientific method principles, it takes just one invalidating piece of data to invalidate an entire theory.
Not correct for something as vague a "spectrum theory of oligometastases". In a circumstance like this, you are looking for signal to validate your hypothesis, and there can be many failed experiments that in aggregate do not invalidate the "entire theory".

Not trying to be an RW apologist regarding his social media behavior, but regarding the oligomets model...there is nothing wrong with being wrong so to speak. It's just a different way of thinking and sets a theoretical framework for discrete experimental work (which as you correctly point out, has demonstrated that aggressive tx of oligomets in bCa is usually futile).

I interpret the RNI literature in bCa as indicating that in some small number of patients RNI is beneficial to late outcomes, distant metastases and OS but it is hard to prove, hard to tell exactly which patients will benefit and these patients will continue to vary in time contingent on screening approaches and systemic therapy.

Even treating the primary alone demonstrates clear clinical signal in metastatic pCa and RCC. Our metastatic models continue to be lacking.
 
Agree with above. Oligomets was actually probably correct just not in breast cancer. (Lung with solitary brain, colorectal with liver, renal cell, melanoma, etc etc etc )

Not sure how RNI got into the conversation. Almost all cancers are still potentially curable with microscopic regional nodal disease
 
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Agree with above. Oligomets was actually probably correct just not in breast cancer. (Lung with solitary brain, colorectal with liver, renal cell, melanoma, etc etc etc )

Not sure how RNI got into the conversation. Almost all cancers are still potentially curable with microscopic regional nodal disease
RNI is always mentioned on this board, every time we talk about breast.
 
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Agree with above. Oligomets was actually probably correct just not in breast cancer. (Lung with solitary brain, colorectal with liver, renal cell, melanoma, etc etc etc )

Not sure how RNI got into the conversation. Almost all cancers are still potentially curable with microscopic regional nodal disease
Again my point, which I think I was somewhat careful to make, is that Ralph didn’t come up with an oligomets theory… he came up with a breast oligomets theory. As far as I know, he never addressed the competing theory which has more data in support. And I don’t think he’s ever attempted to modify the theory or to retract the theory in the face of negative experiments. If he has he’s not done this as publicly as the flag planting editorial which established the theory. This is an editorial that has been cited over 2800 times. I find that a little scientifically impure. Or scientifically chicken s**t.


RNI is always mentioned on this board, every time we talk about breast.

corvette deal with it GIF
I don’t mind bringing up RNI in a breast oligomets convo. There’s no (easy) logical way the breast RNI data can support the breast oligomets theory. Given that the randomized RNI data doesn’t improve OS, data that positive axillary nodes left behind are done so sans harm, and data that about one in two to three women getting RNI have a detectable cancer cell in their marrow… no I don’t mind 😉
 
He definitely thinks we need to get paid closer to pediatricians, a comment he made on Twitter a couple years ago 🤷🏾.

Happy to lift all boats (I do think peds is underpaid) but that doesn't mean letting boomers ride the good times and telling the rest of us that we are paid too much.

But has he at least offered to reduce his own salary down to that of a pediatrician going forward?
 
Likely because back in those days (90s) >90% of patients with stage IV NSCLC, colorectal, ovarian, melanoma died within a year or so, irrelevant if oligometastatic or not. Renal cell might have been the exception due to sometimes very benign course of disease, but it's a rare disease anyhow.

Breast cancer on the other hand was a whole different ball game. Patients with metachronous metastatic breast cancer with favorable biology (luminal A) with bone mets could even back then live for a decade or longer, sometimes only on endocrine therapy. I guess this is what drove the idea behind oligometastasis in breast cancer: Suggesting that aggressive local treatment of mets in oligometastatic breast cancer could enhance survival. 30 years later we now understand that it was likely not the local therapy, but the biology of the disease itself.

And it is the biology that we still do not understand today. We do not really know which stage IV NSCLC, colorectal, ovarian, melanoma patients will benefit from aggressive treatment of mets, or not. Solely a few trials were run in biology-defined subgroups. We have for instance randomized evidence that oligomets treatment enhances OS in EGFRm NSCLC. But we don't decide which melanoma or CRC patient get's oligometastatic treatment based on the biology of the tumor.
The vast biological diversity of cancers is a great point. Even within the same patient, different metastatic sites are often genetically distinct.

It's easy to count mets, it's much harder to understand them biologically.

I heard a good lecture about a year or so ago, that one of the better predictors of progression after oligometastases treatment, isn't just the absolute number but also the rate at which lesions are manifesting.

If more than 3 lesions are popping up each year, it's no longer oligometastases, it's getting away from you. The lecture was given by Ralph W in Chicago.

I think it's too early to sound the death knell for curative intent treatment of oligometastases, but we need better biomarkers of what that truly is, just like we did with HER2 and EGFR and PDL1.

Just curious, any utility of CTCs or Cell-free DNA, or genomic signatures, akin to Oncotype or Decipher, but in oligomets?
 
Not correct for something as vague a "spectrum theory of oligometastases". In a circumstance like this, you are looking for signal to validate your hypothesis, and there can be many failed experiments that in aggregate do not invalidate the "entire theory".

Not trying to be an RW apologist regarding his social media behavior, but regarding the oligomets model...there is nothing wrong with being wrong so to speak. It's just a different way of thinking and sets a theoretical framework for discrete experimental work (which as you correctly point out, has demonstrated that aggressive tx of oligomets in bCa is usually futile).

I interpret the RNI literature in bCa as indicating that in some small number of patients RNI is beneficial to late outcomes, distant metastases and OS but it is hard to prove, hard to tell exactly which patients will benefit and these patients will continue to vary in time contingent on screening approaches and systemic therapy.

Even treating the primary alone demonstrates clear clinical signal in metastatic pCa and RCC. Our metastatic models continue to be lacking.
I wonder if it's like brain mets treated with SRS. Patients with a single brain met do better, and there is an OS benefit to treating single mets with SRS plus whole brain, right? Old RTOG study, 9508.

Gamma Knife series out of Japan also show that solitary mets patients do the best and are their own group. Among patients treated with SRS for 2 to 9 mets vs 10 or more, outcomes are not substantially different. Yamamoto?

Maybe oligo should mean 1, if we're looking to show a really strong benefit.
 
The vast biological diversity of cancers is a great point. Even within the same patient, different metastatic sites are often genetically distinct.

It's easy to count mets, it's much harder to understand them biologically.

I heard a good lecture about a year or so ago, that one of the better predictors of progression after oligometastases treatment, isn't just the absolute number but also the rate at which lesions are manifesting.

If more than 3 lesions are popping up each year, it's no longer oligometastases, it's getting away from you. The lecture was given by Ralph W in Chicago.

I think it's too early to sound the death knell for curative intent treatment of oligometastases, but we need better biomarkers of what that truly is, just like we did with HER2 and EGFR and PDL1.

Just curious, any utility of CTCs or Cell-free DNA, or genomic signatures, akin to Oncotype or Decipher, but in oligomets?
 

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I wonder if it's like brain mets treated with SRS. Patients with a single brain met do better, and there is an OS benefit to treating single mets with SRS plus whole brain, right? Old RTOG study, 9508.
The Andrews trial was provocative back then, but its results have been challenged in subsequent trials, for instance

 
This is a crazy open space. Start-ups (often with academics as leadership or on board) accessing large numbers of patients from academics for black box AI work.

DCISionRT is this sort of tool (AI not doing image analysis on slides for DCISionRT, but did do non-linear modeling using common molecular and clinicopathological features). I would say that the DCISionRT folks did strategically pick a good clinical space (traditional tools for assessing DCIS recurrence risk are pretty bad).

Conversely, Oncotype (not an AI generated tool) probably adds close to nothing in ER/PR+, low ki-67 patients.

I kinda feel that this (AI generated) stuff should all become public domain (particularly if the preponderance of patients were Medicare patients).
 
The reason there are still papers on nodal (ir)radiation in 2025 (do you have a time machine 😉) is hidden within this equivocating apologia. There are some twists and turns, for sure, but...

1) Under usual scientific method principles, it takes just one invalidating piece of data to invalidate an entire theory. That has now happened with NRG BR002 and CURB vis-à-vis Ralph's oligomet theory. They're randomized trials; supposedly we use these to prove/disprove things in medicine, science, etc. (We have even ASCO lit "saying" don't use ablative therapies on M1 breast cancer patients outside of trials... "off-protocol use of [SBRT for breast oligomets], which could have significant toxicity, should probably stop.") The standard of care for M1 breast cancer was never SBRT until one, we had the oligometastatic theory which was mostly "feelings based," and two, we had the tech, and three, probably a sprinkle of SABR-COMET (which was arguably itself a poor reason to use SBRT in M1 breast as N<20 for breast patients there iirc).
2) Re: https://www.thelancet.com/journals/lanepe/article/PIIS2666-7762(24)00329-6/fulltext,
a) not a randomized trial
b) the Danish data has always been an "IMN benefit outlier"
c) The DBCG IMN2 data is population data from ~5000 patients suggesting right sided patients who got IMN RT had a better survival than left sided patients who did not get IMN RT, suggesting OS "causality" linked to IMN RT. What if I had population data from ~7 million patients showing that right sided breast patients already have a built-in survival advantage versus left sided patients; i.e., the IMN RT may very well be a red herring for OS benefit in this "study."
d) Not a single randomized nodal irradiation trial has shown an OS benefit for nodal RT. Not a single randomized IMN RT trial has shown an OS benefit to IMN RT. Both of these findings "fit" much better with the alternative hypothesis versus the oligomet hypothesis.

Here are the tenets of the spectrum hypothesis (outlined by Fisher)
Table 3. The Spectrum Hypothesis (1994)
A third hypothesis [the spectrum thesis] considers breast cancer to be a heterogeneous disease that can be thought of as a spectrum of proclivities [tendencies] extending from a disease that remains local throughout its course to one that is systemic when first detectable.
This hypothesis suggests that metastases are a function of tumor growth and progression.
Lymph node involvement is of prognostic importance not only because it indicates a more malignant tumor biology, but also because persistent disease in the lymph nodes can be the source of distant disease.
This model requires that there are meaningful clinical situations in which lymph nodes are involved, but there has not yet been any distant disease.
Persistent disease, locally or regionally, may give rise to distant metastases and, therefore, in contrast to the systemic theory, locoregional therapy is important.
This third, or spectrum, theory suggests that even if, as the systemic theory suggests, tumor cells spread distantly early in the natural history of the disease, metastases do not regularly occur.
A most important parameter determining the likelihood of their presentation [metastases] is tumor size.
Therefore, there are significant times in the clinically relevant natural history of the disease when metastases have not occurred, but, if the tumor is left inadequately treated, metastases will occur.

There is nothing that I can see has been definitely "disproven". The truth is, the spectrum/oligomet theory and alternative hypothesis have more in common than they have differences. BR-002 and CURB are negative for the application of detecting oligomets with conventional imaging in breast cancer and treating with SBRT in the same way all the initial immunotherapy trials were negative for the application IL-2. A negative trial doesn't invalidate a whole theory, it invalidates the application of the theory of those specific trials.
 
Here are the tenets of the spectrum hypothesis (outlined by Fisher)
Table 3. The Spectrum Hypothesis (1994)
A third hypothesis [the spectrum thesis] considers breast cancer to be a heterogeneous disease that can be thought of as a spectrum of proclivities [tendencies] extending from a disease that remains local throughout its course to one that is systemic when first detectable.
This hypothesis suggests that metastases are a function of tumor growth and progression.
Lymph node involvement is of prognostic importance not only because it indicates a more malignant tumor biology, but also because persistent disease in the lymph nodes can be the source of distant disease.
This model requires that there are meaningful clinical situations in which lymph nodes are involved, but there has not yet been any distant disease.
Persistent disease, locally or regionally, may give rise to distant metastases and, therefore, in contrast to the systemic theory, locoregional therapy is important.
This third, or spectrum, theory suggests that even if, as the systemic theory suggests, tumor cells spread distantly early in the natural history of the disease, metastases do not regularly occur.
A most important parameter determining the likelihood of their presentation [metastases] is tumor size.
Therefore, there are significant times in the clinically relevant natural history of the disease when metastases have not occurred, but, if the tumor is left inadequately treated, metastases will occur.

There is nothing that I can see has been definitely "disproven". The truth is, the spectrum/oligomet theory and alternative hypothesis have more in common than they have differences. BR-002 and CURB are negative for the application of detecting oligomets with conventional imaging in breast cancer and treating with SBRT in the same way all the initial immunotherapy trials were negative for the application IL-2. A negative trial doesn't invalidate a whole theory, it invalidates the application of the theory of those specific trials.
I'm always wary of "the truth is" statements 😉 Bernie might roll over in his grave hearing spectrum vs alternative is more similar than not.

"Unlike the tenets of the alternative hypothesis, which were based on laboratory and clinical investigation, the spectrum hypothesis [ed note: table above] consists of a heterogeneous collection of empirical thoughts and generalities." As we all know, empirical thoughts and generalities are useless to prove a theory/hypothesis either right or wrong. Maybe I shouldn't say breast oligomets hypothesis is disproven. Maybe better to say any treatments based on the hypothesis are unproven. (And yet many, many breast cancer experts across the country tomorrow will be SBRT'ing some M1 breast ca patients.) A theory is only as good as the predictions it makes. "Variations in local-regional therapy are unlikely to substantially affect survival” is a Fisherian prediction. It thus far has been rather incredibly predictive, batting near a thousand. The spectrum hypothesis (MA20, EORTC 22922, CURB, BR002, KROG 0806) is batting close to zero (exception: meta-analysis, but as we also know this weights the Danish data heavily).

LATE EDIT:
Don't sentinel node biopsy low risk breast cancers. And by logical extension no RNI for low-risk cN0/pNx breast cancers. If a rad onc doesn't like Z0011, they may REALLY not like this data (data which fits the alternative hypothesis).
 
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I missed that the prospect trial was published in rectal last year. Almost no indications left in gi
I still treat a ton of low lying rectal cancer/patients hoping for nonoperative cure. Though, yeah, that's about it in gi other than a recent post op pancreas and the occasional esophageal squam. And a couple t4 colons. And liver sbrt
 
Yupp the NYU ad people all procedural specialties, cardiothoracic, neurosurgery, orthopedics. Their hospitals have so much money and such good insurance rates with their hospital fees and academic halo that $8M Super Bowl ad is nothing.

Not a ppse but still a bad actor. Expanding into wealthy area of Florida because that really advances the education & research mission. Definitely not a money grab.
 
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NYU is interesting considering they promoted a rad onc to lead their MD/PhD program a small number of years ago and then cancelled the MD/PhD program entirely with no new students this year (rescinded acceptances) and rumors that there will be no more admits in future years. Academics is no longer very academic at a lot of these places.
 
Yupp the NYU ad people all procedural specialties, cardiothoracic, neurosurgery, orthopedics. Their hospitals have so much money and such good insurance rates with their hospital fees and academic halo that $8M Super Bowl ad is nothing.

Not a ppse but still a bad actor. Expanding into wealthy area of Florida because that really advances the education & research mission. Definitely not a money grab.
NY Presbyetrian/Columbia/Cornell receives 100,000k for 28 fraction prostate from some medicare advantage plans. These systems are trying to capture distant pts from lower cost more efficient community centers.

Re: 4% profit margin: thats an accounting trick. They overhire, overpay admins, overspend to drive margin close to 0.
 
NY Presbyetrian/Columbia/Cornell receives 100,000k for 28 fraction prostate from some medicare advantage plans. These systems are trying to capture distant pts from lower cost more efficient community centers.

NONSENSE.

Certainly seem to be some inefficiencies in the market regarding preferential payments made to certain large institutions or certain types of institutions, created by government policy. If only we had a government department of efficiency (maybe we could call it GDOE or something?) that could look into it.
 
NYU is interesting considering they promoted a rad onc to lead their MD/PhD program a small number of years ago and then cancelled the MD/PhD program entirely with no new students this year (rescinded acceptances) and rumors that there will be no more admits in future years. Academics is no longer very academic at a lot of these places.
No money in research/NIH. Why do robbers rob banks?
 
poor decision by NYU to do those ads. Back in 2012, not so long ago, they had their cancer center shut down after Sandy, and were laying off oncologists.
 
As we try to find a set single place to work for a whole career, find a place where we are valued and have autonomy, deal with some erosion in our specialty's place in oncology (especially if you're a lung cancer rad onc), deal with eroding pay and constant billing/coding changes, deal with our personal tics, foibles, and affectations.... social media for a rad onc can be dicey!

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LOL. These academic divas start tagging the employers. Pure drama *grabs popcorn*


I would tag Drew's employers too TBH. I'm not a lawyer. But a doctor publicly calling another doctor dangerous and a liar ("gaslighting"), and that they are not "in it" for patients... feels like a tort.
 
I suspect a lot of this is for the Twitteratti and they get along just fine in real life.

At the meetings and panels I attend, there’s really no beef between TSurg and rad onc… the reason being, it’s usually not resectability that determines whether or not a surgeon can operate. Most non-operative patients are medically inoperable due to comorbidities. Even if the pharma found a magical neoadj regimen that converted T4N3 patients to ressectable, how many T4N3 could tolerate an operation?
 
I suspect a lot of this is for the Twitteratti and they get along just fine in real life.

At the meetings and panels I attend, there’s really no beef between TSurg and rad onc… the reason being, it’s usually not resectability that determines whether or not a surgeon can operate. Most non-operative patients are medically inoperable due to comorbidities. Even if the pharma found a magical neoadj regimen that converted T4N3 patients to ressectable, how many T4N3 could tolerate an operation?
Agree. Really pulmonary is playing referee in a lot of these cases in my experience. Some will refer straight to us if high risk surgical/bx candidate
 
I suspect a lot of this is for the Twitteratti and they get along just fine in real life.

At the meetings and panels I attend, there’s really no beef between TSurg and rad onc… the reason being, it’s usually not resectability that determines whether or not a surgeon can operate. Most non-operative patients are medically inoperable due to comorbidities. Even if the pharma found a magical neoadj regimen that converted T4N3 patients to ressectable, how many T4N3 could tolerate an operation?
Same.

I’ve got a fantastic thoracic surgeon that is 90% cancer focused and he’s fantastic. We don’t argue. He’s very selective (and wise) about N2 cases.

In my neck of the woods too there’s plenty of obesity and cardiac issues…so lots of reasons not to operate. Maybe in NYC or LA you e got more fit lung patients?
 
Anyone smart know what the chances are and how bad this can get for us?

 
Anyone smart know what the chances are and how bad this can get for us?


Frankly the Trump administration is shocked that physicians haven’t thanked them for cuts and also wanted to remind them they have no
Leverage.
 
Anyone smart know what the chances are and how bad this can get for us?


idk how much change is actually possible for them to pull off but for sure RFK/Elon/Doge are not fans of paying doctors more. only less.
 
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